The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Brandi Pennock - One of the best experts on this subject based on the ideXlab platform.
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resveratrol alleviates Alcoholic Fatty Liver in mice
American Journal of Physiology-gastrointestinal and Liver Physiology, 2008Co-Authors: Joanne M Ajmo, Christopher Q Rogers, Xiaomei Liang, Brandi PennockAbstract:Alcoholic Fatty Liver is associated with inhibition of sirtuin 1 (SIRT1) and AMP-activated kinase (AMPK), two critical signaling molecules regulating the pathways of hepatic lipid metabolism in animals. Resveratrol, a dietary polyphenol, has been identified as a potent activator for both SIRT1 and AMPK. In the present study, we have carried out in vivo animal experiments that test the ability of resveratrol to reverse the inhibitory effects of chronic ethanol feeding on hepatic SIRT1-AMPK signaling system and to prevent the development of Alcoholic Liver steatosis. Resveratrol treatment increased SIRT1 expression levels and stimulated AMPK activity in Livers of ethanol-fed mice. The resveratrol-mediated increase in activities of SIRT1 and AMPK was associated with suppression of sterol regulatory element binding protein 1 (SREBP-1) and activation of peroxisome proliferator-activated receptor γ coactivator α (PGC-1α). In parallel, in ethanol-fed mice, resveratrol administration markedly increased circulating adiponectin levels and enhanced mRNA expression of hepatic adiponectin receptors (AdipoR1/R2). In conclusion, resveratrol treatment led to reduced lipid synthesis and increased rates of Fatty acid oxidation and prevented Alcoholic Liver steatosis. The protective action of resveratrol is in whole or in part mediated through the upregulation of a SIRT1-AMPK signaling system in the Livers of ethanol-fed mice. Our study suggests that resveratrol may serve as a promising agent for preventing or treating human Alcoholic Fatty Liver disease.
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resveratrol alleviates Alcoholic Fatty Liver in mice
American Journal of Physiology-gastrointestinal and Liver Physiology, 2008Co-Authors: Joanne M Ajmo, Christopher Q Rogers, Xiaomei Liang, Brandi PennockAbstract:Alcoholic Fatty Liver is associated with inhibition of sirtuin 1 (SIRT1) and AMP-activated kinase (AMPK), two critical signaling molecules regulating the pathways of hepatic lipid metabolism in animals. Resveratrol, a dietary polyphenol, has been identified as a potent activator for both SIRT1 and AMPK. In the present study, we have carried out in vivo animal experiments that test the ability of resveratrol to reverse the inhibitory effects of chronic ethanol feeding on hepatic SIRT1-AMPK signaling system and to prevent the development of Alcoholic Liver steatosis. Resveratrol treatment increased SIRT1 expression levels and stimulated AMPK activity in Livers of ethanol-fed mice. The resveratrol-mediated increase in activities of SIRT1 and AMPK was associated with suppression of sterol regulatory element binding protein 1 (SREBP-1) and activation of peroxisome proliferator-activated receptor γ coactivator α (PGC-1α). In parallel, in ethanol-fed mice, resveratrol administration markedly increased circulating adiponectin levels and enhanced mRNA expression of hepatic adiponectin receptors (AdipoR1/R2). In conclusion, resveratrol treatment led to reduced lipid synthesis and increased rates of Fatty acid oxidation and prevented Alcoholic Liver steatosis. The protective action of resveratrol is in whole or in part mediated through the upregulation of a SIRT1-AMPK signaling system in the Livers of ethanol-fed mice. Our study suggests that resveratrol may serve as a promising agent for preventing or treating human Alcoholic Fatty Liver disease.
Christopher D. Byrne - One of the best experts on this subject based on the ideXlab platform.
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tests for diagnosing and monitoring non Alcoholic Fatty Liver disease in adults
BMJ, 2018Co-Authors: Christopher D. Byrne, Janisha Patel, Eleonora Scorletti, Giovanni TargherAbstract:This series of occasional articles provides an update on the best use of key diagnostic tests in the initial investigation of common or important clinical presentations. The series advisers are Steve Atkin, professor of medicine, Weill Cornell Medical College Qatar; and Eric Kilpatrick, division chief, clinical chemistry, Sidra Medical and Research Center, Qatar; honorary professor, department of clinical biochemistry, Hull Royal Infirmary, Hull York Medical School. To suggest a topic for this series, please email us at practice@bmj.com. ### What you need to know At a routine work health check, a 52 year old sedentary computer programmer was found to have a serum alanine aminotransferase (ALT) concentration of 68 IU/L (normal 0-40 IU/L), and a triglyceride concentration of 1.9 mmol/L. His fasting plasma glucose level was 5.8 mmol/L and other basic Liver, renal, and lipid blood tests were normal. He had an unremarkable medical history and took no regular medications, did not smoke, and consumed <7 units of alcohol/week. Clinical examination was unremarkable. His body mass index was 29 kg/m2; waist circumference 102 cm, and blood pressure 134/88 mmHg. A repeat serum ALT measurement remained raised some months later, at 62 IU/L. Non-Alcoholic Fatty Liver disease (NAFLD) is a metabolic Liver disease that encompasses a spectrum of progressive pathological conditions, ranging from non-Alcoholic Fatty Liver (NAFL) to steatohepatitis (NASH), fibrosis, and cirrhosis. When hepatic steatosis occurs in …
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non Alcoholic Fatty Liver disease an emerging driving force in chronic kidney disease
Nature Reviews Nephrology, 2017Co-Authors: Giovanni Targher, Christopher D. ByrneAbstract:Non-Alcoholic Fatty Liver disease (NAFLD) not only affects the Liver, but can also increase the risk of developing extra-hepatic diseases, including type 2 diabetes mellitus, cardiovascular disease and chronic kidney disease (CKD). Here, Targher and Byrne discuss the epidemiologic and mechanistic evidence of a pathogenic link between NAFLD and CKD. Non-Alcoholic Fatty Liver disease (NAFLD) is caused by an accumulation of fat in the Liver; the condition can progress over time to increase the risk of developing cirrhosis, end-stage Liver disease and hepatocellular carcinoma. The prevalence of NAFLD is increasing rapidly owing to the global epidemics of obesity and type 2 diabetes mellitus (T2DM), and NAFLD has been predicted to become the most important indication for Liver transplantation over the next decade. It is now increasingly clear that NAFLD not only affects the Liver but can also increase the risk of developing extra-hepatic diseases, including T2DM, cardiovascular disease and chronic kidney disease (CKD), which have a considerable impact on health-care resources. Accumulating evidence indicates that NAFLD exacerbates insulin resistance, predisposes to atherogenic dyslipidaemia and releases a variety of proinflammatory factors, prothrombotic factors and profibrogenic molecules that can promote vascular and renal damage. Furthermore, communication or 'crosstalk' between affected organs or tissues in these diseases has the potential to further harm function and worsen patient outcomes, and increasing amounts of evidence point to a strong association between NAFLD and CKD. Whether a causal relationship between NAFLD and CKD exists remains to be definitively established.
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epidemiological modifiers of non Alcoholic Fatty Liver disease focus on high risk groups
Digestive and Liver Disease, 2015Co-Authors: Amedeo Lonardo, Christopher D. Byrne, Stefano Bellentani, Curtis K Argo, Stefano Ballestri, Stephen H Caldwell, Helena Cortezpinto, Antonio Grieco, Mariana V Machado, Luca MieleAbstract:An improved understanding of non-Alcoholic Fatty Liver disease epidemiology would lead to identification of individuals at high risk of developing chronic Liver disease and extra-hepatic complications, thus contributing to more effective case finding of non-Alcoholic Fatty Liver disease among selected groups. We aimed to illustrate the epidemiology of non-Alcoholic Fatty Liver disease in high-risk groups, which were identified based on existing literature. To this end, PubMed was searched to retrieve original articles published until May 2015 using relevant and pertinent keywords "nonAlcoholic Fatty Liver disease" and "diabetes", "obesity", "hyperlipidaemia", "familial heterozygous hypobetalipoproteinaemia", "hypertension", "metabolic syndrome", "ethnicity", "family history" or "genetic polymorphisms". We found that age, sex and ethnicity are major physiological modifiers of the risk of non-Alcoholic Fatty Liver disease, along with belonging to "non-Alcoholic Fatty Liver disease families" and carrying risk alleles for selected genetic polymorphisms. Metabolic syndrome, diabetes, obesity, mixed hyperlipidaemia and hypocholesterolaemia due to familial hypobetalipoproteinaemia are the major metabolic modifiers of non-Alcoholic Fatty Liver disease risk. Compared with these metabolic conditions, however, arterial hypertension appears to carry a relatively more modest risk of non-Alcoholic Fatty Liver disease. A better understanding of the epidemiology of non-Alcoholic Fatty Liver disease may result in a more liberal policy of case finding among high-risk groups.
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dorothy hodgkin lecture 2012 non Alcoholic Fatty Liver disease insulin resistance and ectopic fat a new problem in diabetes management
Diabetic Medicine, 2012Co-Authors: Christopher D. ByrneAbstract:Diabet. Med. 29, 1098–1107 (2012) Abstract Non-Alcoholic Fatty Liver disease is now recognized as the hepatic component of the metabolic syndrome. Non-Alcoholic Fatty Liver disease is a spectrum of fat-associated Liver conditions that can result in end-stage Liver disease and the need for Liver transplantation. Simple steatosis, or Fatty Liver, occurs early in non-Alcoholic Fatty Liver disease and may progress to non-Alcoholic steatohepatitis, fibrosis and cirrhosis with increased risk of hepatocellular carcinoma. Prevalence estimates for non-Alcoholic Fatty Liver disease range from 17 to 33% in the general populations and it has been estimated that non-Alcoholic Fatty Liver disease exists in up to 70% of people with Type 2 diabetes. Non-Alcoholic Fatty Liver disease increases risk of Type 2 diabetes and cardiovascular disease. In people with Type 2 diabetes, non-Alcoholic Fatty Liver disease is the most frequent cause (∼80%) of Fatty Liver diagnosed by ultrasound. As non-Alcoholic Fatty Liver disease is strongly associated with insulin resistance, the presence of non-Alcoholic Fatty Liver disease with diabetes often contributes to poor glycaemic control. Consequently, strategies that decrease Liver fat and improve whole-body insulin sensitivity may both contribute to prevention of Type 2 diabetes and to better glycaemic control in people who already have developed diabetes. This review summarizes the Dorothy Hodgkin lecture given by the author at the 2012 Diabetes UK annual scientific conference, proposing that Fatty acid fluxes through the Liver are crucial for the pathogenesis of non-Alcoholic Fatty Liver disease and for increasing insulin resistance.
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non Alcoholic Fatty Liver disease a new and important cardiovascular risk factor
European Heart Journal, 2012Co-Authors: Lokpal Bhatia, Nick Curzen, Christopher D. Byrne, Philip C CalderAbstract:Non-Alcoholic Fatty Liver disease (NAFLD) affects up to a third of the population worldwide and may confer increased cardiometabolic risk with consequent adverse cardiovascular outcomes independent of traditional cardiovascular risk factors and the metabolic syndrome. It is characterized almost universally by insulin resistance and is strongly associated with type 2 diabetes and obesity. Non-Alcoholic Fatty Liver disease is a marker of pathological ectopic fat accumulation combined with a low-grade chronic inflammatory state. This results in several deleterious pathophysiological processes including abnormal glucose, Fatty acid and lipoprotein metabolism, increased oxidative stress, deranged adipokine profile, hypercoaguability, endothelial dysfunction, and accelerated progression of atherosclerosis. This ultimately leads to a dysfunctional cardiometabolic phenotype with cardiovascular mortality representing the main mode of premature death in NAFLD. This review is aimed at introducing NAFLD to the clinical cardiologist by discussing in-depth the evidence to date linking NAFLD with cardiovascular disease, reviewing the likely mechanisms underlying this association, as well as summarizing from a cardiologist's perspective, current and potential future treatment options for this increasingly prevalent disease.
Joanne M Ajmo - One of the best experts on this subject based on the ideXlab platform.
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resveratrol alleviates Alcoholic Fatty Liver in mice
American Journal of Physiology-gastrointestinal and Liver Physiology, 2008Co-Authors: Joanne M Ajmo, Christopher Q Rogers, Xiaomei Liang, Brandi PennockAbstract:Alcoholic Fatty Liver is associated with inhibition of sirtuin 1 (SIRT1) and AMP-activated kinase (AMPK), two critical signaling molecules regulating the pathways of hepatic lipid metabolism in animals. Resveratrol, a dietary polyphenol, has been identified as a potent activator for both SIRT1 and AMPK. In the present study, we have carried out in vivo animal experiments that test the ability of resveratrol to reverse the inhibitory effects of chronic ethanol feeding on hepatic SIRT1-AMPK signaling system and to prevent the development of Alcoholic Liver steatosis. Resveratrol treatment increased SIRT1 expression levels and stimulated AMPK activity in Livers of ethanol-fed mice. The resveratrol-mediated increase in activities of SIRT1 and AMPK was associated with suppression of sterol regulatory element binding protein 1 (SREBP-1) and activation of peroxisome proliferator-activated receptor γ coactivator α (PGC-1α). In parallel, in ethanol-fed mice, resveratrol administration markedly increased circulating adiponectin levels and enhanced mRNA expression of hepatic adiponectin receptors (AdipoR1/R2). In conclusion, resveratrol treatment led to reduced lipid synthesis and increased rates of Fatty acid oxidation and prevented Alcoholic Liver steatosis. The protective action of resveratrol is in whole or in part mediated through the upregulation of a SIRT1-AMPK signaling system in the Livers of ethanol-fed mice. Our study suggests that resveratrol may serve as a promising agent for preventing or treating human Alcoholic Fatty Liver disease.
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resveratrol alleviates Alcoholic Fatty Liver in mice
American Journal of Physiology-gastrointestinal and Liver Physiology, 2008Co-Authors: Joanne M Ajmo, Christopher Q Rogers, Xiaomei Liang, Brandi PennockAbstract:Alcoholic Fatty Liver is associated with inhibition of sirtuin 1 (SIRT1) and AMP-activated kinase (AMPK), two critical signaling molecules regulating the pathways of hepatic lipid metabolism in animals. Resveratrol, a dietary polyphenol, has been identified as a potent activator for both SIRT1 and AMPK. In the present study, we have carried out in vivo animal experiments that test the ability of resveratrol to reverse the inhibitory effects of chronic ethanol feeding on hepatic SIRT1-AMPK signaling system and to prevent the development of Alcoholic Liver steatosis. Resveratrol treatment increased SIRT1 expression levels and stimulated AMPK activity in Livers of ethanol-fed mice. The resveratrol-mediated increase in activities of SIRT1 and AMPK was associated with suppression of sterol regulatory element binding protein 1 (SREBP-1) and activation of peroxisome proliferator-activated receptor γ coactivator α (PGC-1α). In parallel, in ethanol-fed mice, resveratrol administration markedly increased circulating adiponectin levels and enhanced mRNA expression of hepatic adiponectin receptors (AdipoR1/R2). In conclusion, resveratrol treatment led to reduced lipid synthesis and increased rates of Fatty acid oxidation and prevented Alcoholic Liver steatosis. The protective action of resveratrol is in whole or in part mediated through the upregulation of a SIRT1-AMPK signaling system in the Livers of ethanol-fed mice. Our study suggests that resveratrol may serve as a promising agent for preventing or treating human Alcoholic Fatty Liver disease.
Xiaomei Liang - One of the best experts on this subject based on the ideXlab platform.
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resveratrol alleviates Alcoholic Fatty Liver in mice
American Journal of Physiology-gastrointestinal and Liver Physiology, 2008Co-Authors: Joanne M Ajmo, Christopher Q Rogers, Xiaomei Liang, Brandi PennockAbstract:Alcoholic Fatty Liver is associated with inhibition of sirtuin 1 (SIRT1) and AMP-activated kinase (AMPK), two critical signaling molecules regulating the pathways of hepatic lipid metabolism in animals. Resveratrol, a dietary polyphenol, has been identified as a potent activator for both SIRT1 and AMPK. In the present study, we have carried out in vivo animal experiments that test the ability of resveratrol to reverse the inhibitory effects of chronic ethanol feeding on hepatic SIRT1-AMPK signaling system and to prevent the development of Alcoholic Liver steatosis. Resveratrol treatment increased SIRT1 expression levels and stimulated AMPK activity in Livers of ethanol-fed mice. The resveratrol-mediated increase in activities of SIRT1 and AMPK was associated with suppression of sterol regulatory element binding protein 1 (SREBP-1) and activation of peroxisome proliferator-activated receptor γ coactivator α (PGC-1α). In parallel, in ethanol-fed mice, resveratrol administration markedly increased circulating adiponectin levels and enhanced mRNA expression of hepatic adiponectin receptors (AdipoR1/R2). In conclusion, resveratrol treatment led to reduced lipid synthesis and increased rates of Fatty acid oxidation and prevented Alcoholic Liver steatosis. The protective action of resveratrol is in whole or in part mediated through the upregulation of a SIRT1-AMPK signaling system in the Livers of ethanol-fed mice. Our study suggests that resveratrol may serve as a promising agent for preventing or treating human Alcoholic Fatty Liver disease.
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resveratrol alleviates Alcoholic Fatty Liver in mice
American Journal of Physiology-gastrointestinal and Liver Physiology, 2008Co-Authors: Joanne M Ajmo, Christopher Q Rogers, Xiaomei Liang, Brandi PennockAbstract:Alcoholic Fatty Liver is associated with inhibition of sirtuin 1 (SIRT1) and AMP-activated kinase (AMPK), two critical signaling molecules regulating the pathways of hepatic lipid metabolism in animals. Resveratrol, a dietary polyphenol, has been identified as a potent activator for both SIRT1 and AMPK. In the present study, we have carried out in vivo animal experiments that test the ability of resveratrol to reverse the inhibitory effects of chronic ethanol feeding on hepatic SIRT1-AMPK signaling system and to prevent the development of Alcoholic Liver steatosis. Resveratrol treatment increased SIRT1 expression levels and stimulated AMPK activity in Livers of ethanol-fed mice. The resveratrol-mediated increase in activities of SIRT1 and AMPK was associated with suppression of sterol regulatory element binding protein 1 (SREBP-1) and activation of peroxisome proliferator-activated receptor γ coactivator α (PGC-1α). In parallel, in ethanol-fed mice, resveratrol administration markedly increased circulating adiponectin levels and enhanced mRNA expression of hepatic adiponectin receptors (AdipoR1/R2). In conclusion, resveratrol treatment led to reduced lipid synthesis and increased rates of Fatty acid oxidation and prevented Alcoholic Liver steatosis. The protective action of resveratrol is in whole or in part mediated through the upregulation of a SIRT1-AMPK signaling system in the Livers of ethanol-fed mice. Our study suggests that resveratrol may serve as a promising agent for preventing or treating human Alcoholic Fatty Liver disease.
Christopher Q Rogers - One of the best experts on this subject based on the ideXlab platform.
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resveratrol alleviates Alcoholic Fatty Liver in mice
American Journal of Physiology-gastrointestinal and Liver Physiology, 2008Co-Authors: Joanne M Ajmo, Christopher Q Rogers, Xiaomei Liang, Brandi PennockAbstract:Alcoholic Fatty Liver is associated with inhibition of sirtuin 1 (SIRT1) and AMP-activated kinase (AMPK), two critical signaling molecules regulating the pathways of hepatic lipid metabolism in animals. Resveratrol, a dietary polyphenol, has been identified as a potent activator for both SIRT1 and AMPK. In the present study, we have carried out in vivo animal experiments that test the ability of resveratrol to reverse the inhibitory effects of chronic ethanol feeding on hepatic SIRT1-AMPK signaling system and to prevent the development of Alcoholic Liver steatosis. Resveratrol treatment increased SIRT1 expression levels and stimulated AMPK activity in Livers of ethanol-fed mice. The resveratrol-mediated increase in activities of SIRT1 and AMPK was associated with suppression of sterol regulatory element binding protein 1 (SREBP-1) and activation of peroxisome proliferator-activated receptor γ coactivator α (PGC-1α). In parallel, in ethanol-fed mice, resveratrol administration markedly increased circulating adiponectin levels and enhanced mRNA expression of hepatic adiponectin receptors (AdipoR1/R2). In conclusion, resveratrol treatment led to reduced lipid synthesis and increased rates of Fatty acid oxidation and prevented Alcoholic Liver steatosis. The protective action of resveratrol is in whole or in part mediated through the upregulation of a SIRT1-AMPK signaling system in the Livers of ethanol-fed mice. Our study suggests that resveratrol may serve as a promising agent for preventing or treating human Alcoholic Fatty Liver disease.
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resveratrol alleviates Alcoholic Fatty Liver in mice
American Journal of Physiology-gastrointestinal and Liver Physiology, 2008Co-Authors: Joanne M Ajmo, Christopher Q Rogers, Xiaomei Liang, Brandi PennockAbstract:Alcoholic Fatty Liver is associated with inhibition of sirtuin 1 (SIRT1) and AMP-activated kinase (AMPK), two critical signaling molecules regulating the pathways of hepatic lipid metabolism in animals. Resveratrol, a dietary polyphenol, has been identified as a potent activator for both SIRT1 and AMPK. In the present study, we have carried out in vivo animal experiments that test the ability of resveratrol to reverse the inhibitory effects of chronic ethanol feeding on hepatic SIRT1-AMPK signaling system and to prevent the development of Alcoholic Liver steatosis. Resveratrol treatment increased SIRT1 expression levels and stimulated AMPK activity in Livers of ethanol-fed mice. The resveratrol-mediated increase in activities of SIRT1 and AMPK was associated with suppression of sterol regulatory element binding protein 1 (SREBP-1) and activation of peroxisome proliferator-activated receptor γ coactivator α (PGC-1α). In parallel, in ethanol-fed mice, resveratrol administration markedly increased circulating adiponectin levels and enhanced mRNA expression of hepatic adiponectin receptors (AdipoR1/R2). In conclusion, resveratrol treatment led to reduced lipid synthesis and increased rates of Fatty acid oxidation and prevented Alcoholic Liver steatosis. The protective action of resveratrol is in whole or in part mediated through the upregulation of a SIRT1-AMPK signaling system in the Livers of ethanol-fed mice. Our study suggests that resveratrol may serve as a promising agent for preventing or treating human Alcoholic Fatty Liver disease.